Approximately 25% of the workforce in North America is involved in work outside the usual daytime hours.1 Previous work has shown that night shift work, especially rotating shift work can have detrimental affects both in the short term and long term compared to day shift work. In the short term there is an increased incidence of accidents and impaired job performance due to reduced alertness,2-6 while in the long term there is an increased risk of various forms of cancer including breast, prostate and colorectal carcinoma.7-10 Higher incidence of obesity, cardiac disease and stress related psychosomatic disorders have also been noted in these chronic rotating shift workers.11-13 These adverse health effects are strongly connected to circadian rhythm disruption due to bright light exposure at night. Circadian rhythms exhibit roughly a 24 hour pattern and are observed in various physiological functions including, but not limited to, sleep/wake cycle, feeding times, mood, alertness, cell proliferation and even gene expression in various tissue types.14-16 These rhythms are regulated by the master circadian clock located in the Suprachiasmatic Nuclei (SCN). One key regulator used by the SCN is the neurohormone melatonin, often referred to as the hormone of darkness.17 
Melatonin (N-acetyl-5-methoxytryptamine) is the principal hormone of the pineal gland, and mediates many biological functions, particularly the timing of those physiological functions that are controlled by the duration of light and darkness. Melatonin is synthesized from tryptophan through serotonin, which is N-acetylated by the enzyme n-acetyl transferase or NAT, and then methylated by hydroxyindol-O-methyl transferase. The enzyme NAT is the rate-limiting enzyme for the synthesis of melatonin, and is increased by norepinephrine at the sympathetic nerve endings in the pineal gland. Norepinephrine is released at night or in the dark phase from these nerve endings. Thus, melatonin secretion is controlled mainly by light and dark phases.
Melatonin is secreted from the pineal gland in a diurnal rhythm, peaking at night and its secretion is highly light sensitive. Nocturnal light exposure significantly suppresses melatonin secretion.18-20 Interestingly, the suppressive effect of light on melatonin varies with differing wavelengths, and light of relatively short wavelengths (between 420 to 520 nm) has the most pronounced suppressant effect.21-27 Melatonin has been shown to have various functions such as chronobiotic regulation, immunomodulation, antioxidant effects, regulation of the timing of seasonal breeding and oncostatic effects.28-30 The oncostatic effects of melatonin have been shown in vitro, and in animal studies showing that constant exposure to light significantly promotes carcinogenesis due to melatonin suppression.29,30 Hence, melatonin suppression by nocturnal bright light has been proposed as a key mediator of the adverse affects of rotating shift work.
Furthermore, light at night disrupts many other endocrine networks, most notably glucocorticoids.31 Glucocorticoids are a class of steroid hormone produced in the cortex of the adrenal glands. Cortisol is the most important human glucocorticoid and is associated with a variety of cardiovascular, metabolic, immunologic, and homeostatic functions. Elevated levels of cortisol are associated with a stress response. Light induces gene expression in the adrenal gland via the SCN-sympathetic nervous system and this gene expression is associated with elevated plasma and brain glucocorticoids. The amount of cortisol present in the serum generally undergoes diurnal variation, with the highest levels present in the early morning, and the lowest levels at night. The magnitude of glucocorticoid release by light is also dose dependently correlated with the light intensity. Light-induced clock-dependent secretion of glucocorticoids may serve an adaptive function to adjust cellular metabolism to the light in a night environment, but also illustrates the presence of stress in response to nocturnal lighting. Elevated glucocorticoids pose numerous health risks including hypertension,32 psychiatric disorders,33 elevated blood sugar levels, and suppression of the immune system. Increased glucocorticoid levels have also been linked with faster proliferation rates of various carcinomas, most notably breast cancer.34,35 Elevated levels of cortisol during pregnancy are further associated with metabolic syndrome in offspring. Epidemiological studies in diverse populations have demonstrated an association between low birth weight and the subsequent development of hypertension, insulin resistance, Type 2 diabetes, and cardiovascular disease.36 This association appears to be independent of classical adult lifestyle risk factors.37 In explanation, it has been proposed that a stimulus or insult acting during critical periods of growth and development permanently alters tissue structure and function, a phenomenon termed “fetal programming”. Intriguingly, there is evidence that this phenomenon is not limited to the first-generation offspring and programming effects may persist in subsequent generations. Epidemiological studies in humans suggest intergenerational effects on birth weight, cardiovascular risk factors, and Type 2 diabetes. Similarly, transgenerational effects on birth weight, glucose tolerance, blood pressure, and the hypothalamic-pituitary-adrenal axis have been reported in animal models. One major hypothesis to explain fetal programming invokes overexposure of the fetus to glucocorticoids.38 Glucocorticoids exert long-term organizational effects and regulate organ development and maturation.39,40 In fact, glucocorticoids are exploited therapeutically in the perinatal period to alter the rate of maturation of organs such as the lung.41 Glucocorticoid treatment during pregnancy reduces birth weight in animals and humans.42,43 Furthermore, cortisol levels are increased in human fetuses with intrauterine growth retardation or in pregnancies complicated by preeclampsia, which may reflect a stress response in the fetus.44 It has been shown that rats exposed to dexamethasone (synthetic glucocorticoid) during the last third of pregnancy, are of low birth weight and develop hypertension and glucose intolerance in adulthood.45-48 
The chronobiotic properties of melatonin can synchronize overall circadian rhythms. In the absence of melatonin there can be desynchronization of the biological clock because the phase or timing of physiological processes does not align with external time queues. Such an example is the markedly delayed time of sleep onset and offset in patients with Delayed Sleep Phase Syndrome (DSPS), which does not correspond to habitual hours of sleep and activity. These individuals exhibit poor alertness and psychomotor performance when they are made to conform to conventional times of activity. Furthermore, such underlying circadian rhythm misalignment can often manifest itself as overt psychological disorders ranging from subsyndromal depression to major depression.
The presence of depression in DSPS populations has been previously reported.49 DSPS is characterised by sleep onset insomnia where the patient may spend long hours before being able to fall asleep. It is a Circadian Rhythm Sleep Disorder, caused by a desynchronized central biological clock. It has been reported that DSPS patients showed emotional features such as low self esteem, nervousness and lack of control of emotional expression. These characteristics may worsen social withdrawal, causing a loss of social cues in synchronizing their circadian rhythm. Thus, the phase shift becomes more profound and a vicious circle continues.
Apart from psychological disorders in individuals with circadian rhythm misalignment, the presence of depression has also been noted in low melatonin secretors. Wetterberg50 postulated that low melatonin secretion can be a biological marker for susceptibility to endogenous depression. The clinical symptoms of depressed mood seen in his patients included insomnia, psychomotor retardation, poor memory and concentration and suicidal thoughts. Several studies undertaken in recent years have also shown that both the amplitude and rhythm of melatonin secretion is altered in patients suffering from unipolar depression as well as in patients suffering from bipolar affective disorders.51,52 
Such rhythm disturbances and associated pathologies are of major concern not only in adults but in adolescents too.53 Given their post-pubescent hormonal system that is constantly changing along with multi-faceted social demands and poor sleep hygiene, circadian rhythm disruptions can pose as a significant threat to their overall well being.54 Although limited in numbers, epidemiological and clinical research of sleep in adolescents shows alarming trends. A major study showed that adolescents need 8.5-9.25 hours sleep per night.55 The same researchers, in a survey of 3,120 high school students, found those who reported grades as C, D or F had 25 minutes less sleep on week nights than those reporting A or B grades.56 A survey of 3,400 high school students in Ontario, Canada showed that 47.3% of students had less than 8 hours sleep on week nights and 60-70% reported that they were often very sleepy between 8-10 A.M., raising concern about school start time and academic scheduling.57 The same study found a positive linear relationship between increased daytime “sleepiness” and decreased academic and extracurricular performance. These findings indicate a potentially significant health problem and impact on educational achievement. The survey results suggest that of the approximately 2 million Canadians aged 14-18, there could be as many as 115,000 adolescents with unrecognized medical sleep disorders and at least 975,000 with significant sleep deprivation; a major portion of these sleep disorders can be attributed to circadian rhythm disruption.57 These findings stress the need for rectifying circadian rhythm misalignment in adolescents to help these young individuals in achieving their full potential.
Exposure to bright light at night can desynchronize the SCN, the master circadian clock leading to the mistiming of various physiological functions resulting in poor health.
One of the major approaches taken to improve conditions associated with disruption of the usual light-dark cycle include entrainment of the circadian rhythm to a delayed phase using bright light therapy in the hopes of increasing alertness at night and inducing sleep during morning hours.58-61 However, at the end of the night shift exposure to bright daylight serves as a potent Zeitgeber, overriding the potentially beneficial effects of bright light interventions and negating circadian rhythm entrainment.62 Additionally, bright light administered at night disrupts the body's natural circadian melatonin profile by preventing the melatonin secretion at night. Substantial research evidence is emerging to implicate potential long term consequences of shift-work associated risk factors including increased risk of cancer, cardiovascular disease, gastrointestinal disorders and mood disorders and their associated morbidity and mortality. Recent studies implicate melatonin secretion disruption with these risk factors.
As an example of one of these known approaches, U.S. Pat. No. 5,304,212 to Czeisler et al. teaches a method for modifying the endogenous circadian pacemaker involving the timed application of light.
U.S. Pat. No. 6,638,963 to Lewy et al. teaches a method for treating circadian rhythm disorders including shift work-related desynchronies that involves the administration of melatonin, melatonin agonists or compounds that stimulate endogenous melatonin production. This type of pharmaceutical based intervention is inevitably associated with compliance problems (including problems related to financial difficulties) and side effect risks.
Most steroid-type hormones have a short half-life, so a large dose or multiple doses would be required to mimic the normal nocturnal rise in a subject. The appropriate dose for this type of pharmaceutical intervention is not known and there is the possibility of side effects or unknown toxicity depending on the purity of the melatonin product used.
U.S. Pat. No. 6,156,743 to Whitcomb teaches a method of decreasing fatigue in humans who are shifting their time of wakefulness (e.g. night shift workers) by administering an effective amount of hydrocortisone (i.e. pharmaceutical cortisol.) While administration of hydrocortisone may be associated with short-term relief from fatigue, as discussed above, elevated levels of cortisol are associated with a number of adverse health effects.
United States patent application publication number 2006/0119954 to Casper et al. (“Casper et al.”), which has common inventors with the present application, provides a device for inhibiting melatonin suppression by selectively blocking light of wavelength less than 530 nm. This invention is directed to the inhibition of melatonin suppression, but not moderating the expression of other genes that exhibit a circadian rhythm expression pattern. Further, while generally a useful level of colour recognition is obtained with these filters, they may give transmitted images a “yellow hue” and render certain colours difficult to distinguish, in particular: white/grey/yellow and blue/green/black.
A publication by Phelps [Phelps J, Dark therapy for bipolar disorder using amber lenses for blue light blockade, Med Hypotheses (2007)] studies the use of amber safety goggles at night as a possible therapy for sufferers of bipolar disorder. Such goggles transmit a limited amount of light: most likely, less than 50% of all wavelengths of light; and generally block all wavelengths of light less than about 530 nm. Consequently, such goggles limit the ability to distinguish between colours, as described with respect to Casper et al., and are not suitable for many industrial applications. Further, while Phelps suggests that the symptoms of the bipolar sufferers might be improved as a result of circadian rhythm effects, this is speculative and is based on known information in the field and observation of the symptoms of the subjects involved in the study.
U.S. Pat. No. 4,878,748 to Johansen et al. teaches sunglasses for blocking horizontally polarized light and blue light, blocking light between 300 and 549 nm, but also substantially blocking light at all wavelengths: less than 50% of the light at wavelengths above the “blocked” range is transmitted. Johansen et al. does not address the problems associated with disruption of the circadian rhythm suffered by those exposed to light at night. The Johansen et al. inventors are concerned with protecting the retina from damage caused by exposure to high intensity daylight.
There is a need for a simple, effective and inexpensive method to prevent the varied adverse health effects of light exposure at night, without unduly increasing fatigue or reducing alertness.